JunB Double Nickase Plasmid (h): sc-400493-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- JunB Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- JunB Double Nickase Plasmid (h) and JunB Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting JUNB. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: JunB Antibody (C-11): sc-8051
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
JunB Double Nickase Plasmid (h) | sc-400493-NIC | 20 µg | $410.00 | |||
JunB Double Nickase Plasmid (h2) | sc-400493-NIC-2 | 20 µg | $410.00 |
JUNB encodes JunB, a leucine zipper transcription factor within the AP-1 complex that integrates MAPK/ERK and JNK signaling to regulate stimulus-dependent gene expression programs. JunB modulates cell-cycle progression, differentiation, and stress and cytokine responses by partnering with FOS family proteins and binding AP-1 motifs across enhancers and promoters. Through these networks it influences immune cell activation and inflammatory signaling, and it is frequently used as a readout of immediate-early transcriptional responses. Dysregulated JUNB activity has been implicated in oncogenic transcriptional rewiring and altered immune phenotypes, supporting its study in tumor biology and inflammation-associated pathways.
JunB Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the JUNB locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within JUNB. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt JUNB function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of JUNB-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.